Cardiovascular System

ISCHAEMIC HEART DISEASE

Ischaemic heart disease (IHD) is defined as 'acute or chronic form of a cardiac disability arising from imbalance between the myocardial supply and demand of oxygenated blood'.

The alternate term coronary artery disease (CAD) is used synonymously with IHD. Depending on the rate and severity of coronary artery narrowing and the myocardial response, one of four syndromes may develop.

• Angina pectoris (Chest pain),

• Acute myocardial infarction,

• Chronic ischemic heart disease with congestive heart failure,

Sudden cardiac death.

Etiology

The most common cause of ischemic heart disease is a reduction in coronary arterial blood supply due to atherosclerosis of the coronary arteries. Factors that contribute to the development of ischaemic heart disease are similar to those responsible for atherosclerosis in general, and include: Hypertension, diabetes mellitus, smoking, high cholesterol, high levels of low density lipoprotein, and genetic factors and non-atherosclerotic causes are vasospasm, coronary artery stenosis, inflammation of coronary arteries, thrombotic disease, trauma, aneurysms and compression.

Pathogenesis

Symptomatic ischemic heart disease is typically associated with a critical stenosis, defined as a 75% or greater reduction in the lumen of one or more coronary arteries by atherosclerotic plaque. With this level of fixed obstruction, the augmented coronary blood follow that may occur as a result of compensatory coronary vasodilation is insufficient to meet even moderate increase in myocardial oxygen demand. In addition to chronic, fixed atherosclerotic plaques, various superimposed lesions also play an important role in the development of myocardial ischemia. These include —

1. Acute changes in the morphology of chronic atherosclerotic plagues include fissuring, haemorrhage into the plaque, and plaque rupture with embolization of atheromataous debris into distal coronary vessels. In addition to causing enlargement of the plaque, local disruption of plaque increases the risk of platelet aggregation and thrombosis at the site.

2. Local plated aggregation in the coronary arteries has been documented in patients with unstable angina pectoris and in patients who undergo sudden cardiac death. Both mechanical occlusion of small blood vessels by small platelet aggregates and coronary vasospasm induced by mediators released from the platelet aggregates may contribute to myocardial ischemia.

3. Coronary artery thrombosis is almost always associated with a severe atherosclerotic plaque. Local disruption of atheromataous plaques plays an important role in the development of thrombi by exposing thrombogenic, lipid rich plaque debris to the blood.

4. Coronary artery spasm usually occurs in patients with at least some pre-existing atherosclerosis. It has been associated with one particular type of angina pectoris, termed Prinzmental’s (variant) angina.

Clinical Manifestations

Depending on the rate and severity of coronary artery narrowing and the myocardial response, one of four syndromes may develop.

1. Angina pectoris (Chest pain),

2. Acute myocardial infarction,

3. Chronic ischemic heart disease with congestive heart failure,

4. Sudden cardiac death.

Prevention

Fatty diet, smoking, sedentary lifestyle and stress should be avoided, as they are the main causes of Ischemic heart diseases. Avoiding food rich in saturated fats is important to reduce lipid levels in the blood and to prevent arteriosclerosis. Adequate regular exercise is also essential. Cholesterol and hypertension should be kept under good control with proper treatment.

Treatment

Organic Nitrates: These stimulates the intracellular cyclic-GMP, which results in vascular smooth muscle relaxation of both arterial and venous vasculature. e.g. Isosorbide dinitrate.

β-Blockers: β-Blockers act by reducing cardiac work and O2 consumption. e.g. Propranolol, Atenolol.

Calcium Channel Blockers: Calcium antagonist inhibits the passage of calcium ions through voltage-dependent L-type calcium channels in cell membranes in the heart and vascular smooth muscle as well as some other excitable tissues. e.g. Amlodipine Nifedipine.

Statins: IHD is also due to the increased cholesterol levels. Statins are used to reduce the cholesterol levels in hyper- cholesterolemia. Statins are the HMG-CoA reductase inhibitors. e.g. Atorvastatin, Rusvastatin.

Aspirin: Aspirin improves the rate of survival in patients with acute myocardial infarction and reduces the risk of myocardial infarction in patients with unstable angina, and after recovery from myocardial infarction.

Angina Pectoris

Angina pectoris is a clinical syndrome of Ischemic heart disease (IHD) resulting from transient myocardial ischaemia if the heart muscle does not get as much blood as it needs. This usually happens because one or more of the heart's arteries is narrowed or blocked. It is characterised by paroxysmal pain in the substernal or precordial region of the chest which is aggravated by an increase in the demand of the heart and relived by a decrease in the work of hear. Often, the pain radiates to the left arm, neck jaw or right arm.

Myocardial Infarction (Heart Attack)

Myocardial Infarction is a condition resulting from decreased blood and oxygen supply to the heart, causing cell death. The major cause is sudden blockage of coronary arteries.

Coronary arteries are blood vessels that supply the heart muscle with blood and oxygen. Blockage of a coronary artery deprives the heart muscle of blood and oxygen, causing injury to the heart muscle causing chest pain and chest pressure sensation.

Etiology

Myocardial infarction (MI) is the irreversible death (necrosis) of heart muscle which usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in an epicardial coronary artery, resulting in an acute reduction of blood supply to a portion of the myocardium.

Pathogenesis
1. Myocardial Ischaemia: Myocardial ischaemia is brought about by one or more of the following mechanisms:

(i) Diminised coronary blood flow e.g. in coronary artery disease shock.

(ii) Increased myocardial demand e.g. In exercise, emotions.

(iii) Hypertrophy of the heart without simultaneous increase of coronary blood flow e.g. in hypertension, valvular heart disease.

2. Role of platelets: Rupture of an atherosclerotic plaque exposes the subendothelial collagen to platelets which undergo aggregation, activation and release reaction. These events contribute to the build-up of the platelet mass that may give rise to emboli or initiate thrombosis.

3. Acute plaque rupture: In general, slowly developing coronary ischaemia from stenosis coronary atherosclerosis of high grade may not cause acute MI but continue to produce episodes of angina pectoris.

4. Non-atherosclerotic causes: About 10% cases of acute MI are caused by non-atherosclerotic factors such as coronary vasospasm, arteritis, coronary l stenosis embolism, thrombotic diseases, trauma and outside compression as already described.

Signs and Symptoms

Patients with typical MI may have the following symptoms in the days or even weeks preceding the event: Fatigue, Chest discomfort, Malaise.

Typical chest pain in acute MI has the following characteristics:

• Intense and unremitting for 30-60 minutes.

• Substernal, and often radiates upto the neck, shoulder, and jaw, and down the left arm.

• Usually described as a substernal pressure sensation that also may be characterized as squeezing, aching, burning, or even sharp.

In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness and gas.

Treatment

Emergency agents: Emergency agents are used in the process of reperfusion of the heart muscle. These agents basically help in relieving the severe heart pain, cause Vasodilatation to open the blocked artery, restore the oxygen supply and prevent the further damage of the heart muscle. These agents are morphine, oxygen, nitroglycerine, aspirin.

Anti-platelet agents: Anti-platelet medications prevent formation of blood clots in the arteries. In NSAID, aspirin inhibits cyclooxygenase-1 enzyme and thus prevents blood clotting by blocking the production of thromboxane A-2 by platelets, the chemical that causes platelets to clump.

Anti-coagulants: Anti-coagulant medications prevent growth of blood clots in the arteries. Anti-coagulants such as intravenous or subcutaneous heparin, subcutaneous low molecular weight heparin, and oral warfarin, prevent the formation of blood clots either by inhibiting the production of clotting factors or by interfering with the action of the clotting factors. e.g. Enoxaparin.

Clot-dissolving medications:

Fibrinolytic or thrombolytic agents are known as clot dissolving agents used to open blocked arteries and dissolve the existing clots.

β-adrenergic receptor blockers: β- blockers act by decreasing the workload of the heart. Decrease in the workload decreases the demand for oxygen by the heart and limits the amount of damage to the heart muscle.